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Primary Care 3 > Endocrine Up to Dates > Flashcards

Endocrine Up to Dates Flashcards

1
Q

The most common clinical presentation of primary hyperparathyroidism

A

asymptomatic hypercalcemia detected by routine blood work

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2
Q

Clinical manifestations of PHPT

A

Skeletal manifestations and kidney stones (nephrocalcinosis)

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3
Q

Physical findings in PHPT

A

usually no physical findings. may have a palpable neck mass but that is most likely a thyroid nodule or parathyroid carcinoma

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4
Q

Normocalcemic primary hyperparathyroidism

A

PTH levels are elevated but the serum calcium is normal. For this diagnosis, all secondary causes for hyperparathyroidism must be ruled out and ionized calcium levels should be normal

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5
Q

Parathyroid crisis

A

Very rare condition. Consists of severe hypercalcemia — above 15 and s/s of hypercalcemia - CNS dysfunction. AMS, bone disease, kidney stones. Can be caused by a life threatening illness, volume loss or an infarction of a parathyroid adenoma

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6
Q

Classic PHPT

A

Combined effects of increased PTH secretion and hypercalcemia. Bones, stones, abdominal moans and psychic groans.

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7
Q

Prolonged PTH excess leads to

A

kidney stones and bone disease

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8
Q

Symptoms of hypercalcemia

A

anorexia, nausea, constipation, polydipsia, polyuria

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9
Q

Most common complication of PHPT

A

kidney stones

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10
Q

Ostitis Fibrosa cystica

A

Most often in those with severe disease or parathyroid carcinoma. Classic manifestation of PHPT bone disease. Characterized by bone pain and radiographically by subperiosteal bone resorption on the radial aspect of the middle phalanges, tapering of distal clavicles and a salt and pepper appearance of the skull, bone cysts, brown tumors of the long bones. Bone tumors are from excess osteoclast activity.

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11
Q

Nephrolithiasis PHPT

A

Kidney stones. Most often comprised of calcium oxalate.

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12
Q

Neuromuscular s/s PHPT

A

Weakness and fatigue. Improved when parathyroid is removed. Bone pain, osteoporosis/osteopenia

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13
Q

Neuropsychiatric symptoms PHPT

A

lethargy, depressed mood, psychosis, decreased social interaction, cognitive dysfunction. Decreased concentration, confusion, stupor, coma

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14
Q

Renal disease s/s PHPT

A

decrease concentrating ability with a GFR less than 60

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15
Q

Cardiovascular s/s PHPT

A

HTN, arrhythmia, ventricular hypertrophy and vascular and valvular calcification

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16
Q

Rhem s/s PHPT

A

hyperuricemia, gout, pseudogout in wrist and knees

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17
Q

Lab findings PHPT

A

hypophosphatemia, decreased mg, anemia which responds to a parathyroidectomy

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18
Q

Causes of secondary hyperparathyroidism

A

Renal failure: hyperphosphatmia/impaired calcitrol production. Calcium malabsorption from vitamin D deficiency, bariatric surgery, celiac disease, pancreatic disease (fat malabsorption). Renal calcium loss from hypercalciuria or loop diuretics. Inhibition of bone resorption through biphosphonates or hungry bone syndrome

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19
Q

PHPT s/s

A

bone disease, kidney stones, hypophosphatemia, increased production of calcitol (Vitamin D3), proximal renal tubular acidosis, hypomagnesmia, hyperuricemia, gout, anemia

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20
Q

GI s/s PHPT

A

Anorexia, n/v, constipation, pancreatitis, Peptic ulcer disease

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21
Q

Renal s/s PHPT

A

polyuria, polydipsia, nephrolithiasis, nephrocalcitonosis, distal tubular acidosis, neprogenic DI, acute and chronic renal insufficiency

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22
Q

cardiovascular s/s PHPT

A

shortened QT interval, bradycardia, hypertension

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23
Q

Treatment options for PHPT

A

surgical intervention vs. observation

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24
Q

Who is surgery recommended for

A

Hyperparathyroidism with symptomatic disease (polyuria, polydipsia, fragility fx, kidney stones, osteoporosis, pud, pancreatitis, gerd, neurodysfunction)

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25
Q

Asymptomatic patient who needs surgery

A

< 50, likely to progress into symptomatic based on GFR, T score < 2.5 (osteoporosis) and calcium greater than 1mg/dL above normal

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26
Q

Parathyroid exploration

A

PHPT as a result of parathyroid cancer or parathyroid crisis, or with recurrent primary hyperparathyroidism

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27
Q

Contraindications to parathyroidectomy

A

contralateral recurrent laryngeal nerve injury and symptomatic cervical disc disease

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28
Q

Complications of parathyroidectomy

A

failure to achieve cure of hypercalcemia, hematoma with airway compromise, hypoparathyroidism and laryngeal nerve injury

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29
Q

subclinical hyperthyroidism

A

no clinical symptoms just a low TSH

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30
Q

overt hyperthyroidism

A

dramatic symptoms – lability, tremors, palpitations, anxiety, sweaty, increased heat intolerance, urinary frequency, hyperdefecation,

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31
Q

mild hyperthyroidism

A

symptoms only to a few organ systems, like weight loss, new afib, menstrual disorders

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32
Q

symptoms of hyperthyroidism is the older adult

A

may have more cardiac and resp symptoms - tachycardia, afib, DOE, apathetic thyrotoxicosis (no symptoms except weakness and asthenia)

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33
Q

physical exam with hyperthryoidism

A

hyperactivity, rapid speech. lid lag/stare. warm skin. thin hair. tachycardia. afib irregular pulse. systolic hypertension. tremor. hyperreflexia. (exophalmus. periorbital edema and limited eye movement only with graves disease)

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34
Q

Subclinical hyperthyroid

A

low tsh but normal t4 t3 free t3 most do not have any clinical s/s of hyperthyroidism Can be mild graves or a multinodular goiter

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35
Q

primary hyperthyroidism labs

A

low tsh, high t3 and/or t4

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36
Q

t3 toxicosis

A

greater increase in t3 than t4, seen in Graves or a nodular goiter. Due to increased t3 secretion and an increased extrathyroidal conversation of t4 to t3

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37
Q

t4 toxicosis

A

low TSH, high t4, normal t3. Found in those with hyperthyroidism with an extrathyroidal condition which decreases conversion of t4 to t3

38
Q

Amiodarone

A

inhibits extrathyroidal conversion of t4 to t3. In patients with amiodarone induced hyperthyroid will have elevated t4 and a t3 not as elevated.

39
Q

Subclinical hyperthyroid

A

low tsh but normal t4 t3 free t3 most do not have any clinical s/s of hyperthyroidism Can be mild graves or a multinodular goiter

40
Q

TSH induced hyperthyroidism

A

very rare, due to TSH secreting pituitary adenoma or a defect in a t3 receptor resisting the feedback of t4 and t3 on TSH secretion. High TSH despite high t4 and t3

41
Q

Central hypothyroidism

A

low TSH and normal but usually low free t4 and t3

42
Q

meds that can cause a low TSH and a low or normal t3 t4

A

high dose glucocorticoids, high dose dopamine

43
Q

TSH in pregnancy

A

physiologically lowers

44
Q

diagnose graves on this criteria - 3 criteria

A

new onset opthamolopathy, large non-nodular thyroid, moderate to sever hyperthyroidism

45
Q

if diagnosis of hyperthyroidism is not apparent based on clinical presentation, these diagnostic tests can be ordered

A

measurement of thyrotropin receptor antibodies, determination of radioactive iodine uptake, measurement of thyroid blood flow via ultrasound

46
Q

trAb + antibodies confirms what

A

graves

47
Q

t3 and t4 high, tsh normal or high…

A

need to evaluate for a pth producing pituitary tumor - need MRI

48
Q

RAI with toxic multinodular goiter

A

areas of increased and suppressed uptake

49
Q

RAI with toxic adenoma

A

focal increased uptake

50
Q

tsh low and only T3 high…

A

graves or thyroid adenoma

51
Q

tsh low and T4 high…

A

hyperthyroid with a nonthyroidal illness, amiodarone, exogenous t4 ingestion

52
Q

t3 and t4 high, tsh normal or high…

A

need to evaluate for a pth producing pituitary tumor - need MRI

53
Q

Hyperthyroid testing for pregnancy

A

no RAI. US or antibodies TRAb.

54
Q

most common cause of hyperthyroidism

A

graves

55
Q

diffuse goiter could indicate

A

graves, painless thyroiditis, TSH secreting pituitary tumor

56
Q

skin and hair w hyperthyroid

A

thin hair, alopecia areata, oncholysis (loosing nails from nail bed) and soft tails, sweating, itching, hives, vitiligo

57
Q

infiltrative dermopathy

A

only in graves, most commonly over the shins, raised, hyperpigmented, orange peel textured papules

58
Q

eyes in hyperthyroid

A

lid lag and stare. Due to overactivity from alpha adrenergic receptors of tissues. Eval by having follow finger up and down with eyes + if the sclera can be seen above the iris as the patient looks downward

59
Q

Opthamalopathy

A

only in graves. Inflammed extraocular muscles and the orbital fat and connective tissue causing proptosis (exopthalmus), impaired eye function and periorbital and conjunctival edema.. can cause diplopia or corneal ulcers

60
Q

cardiovascular s/s hyperthyroid

A

increased heart rate, palpitations, widened pulse pressure, systolic hypertension, can have CHF or a worsened CHF in those who already have it, a fib in 10-20 percent, which usually spontaneously converts, need anticoagulation.

61
Q

serum lipids with hyperthyroid

A

low HDL and low total/HDL ratio

62
Q

hyperglycemia with hyperthyroid

A

interferes with glucose metabolism from increased sensitivity of pancreatic beta cells to glucose leading to impaired glucose tolerace from the increased sensitivity

63
Q

resp with hyperthyroid

A

DOE, dyspnea, from increased o2 consumption, resp muscle weakness, tracheal obstructions from goiters, exacc asthma from hyperthyroidism

64
Q

GI s/s hyperthyroidism

A

weight loss from hypermetabolism, increased gut motility, hyperdefecation, malabsorption, celiac more prevalent with graves. can have increased appetite. can be anorexic if older. may have dysphagia due to a goiter,

65
Q

thymic enlargement

A

in graves this is due to hyperplasia usually discovered for a workup of dyspnea, can be due to autoimmune (thyroid stimulating immunoglobulins binding to the TSH receptor in the thymus leading to thymocyte proliferation

66
Q

treat thymic enlargement

A

antithyroid meds, radioiodine or thyroidectomy – all will treat graves and decrease the enlargement (thyroidectomy to remove it and antithyroid and RAI to kill it)

67
Q

hematologic issues with hyperthyroid

A

plasma volume increased, RBC increased leading to normochromic normocytic anemia. Graves may be a/w other autoimmune disorders like ITP.

68
Q

GU hyperthyroid

A

urinary frequency and nocturia, primary polydipsia, hypercalciurea

69
Q

bone s/s hyperthyroid

A

stimulates bone resorption causing increased porosity of cortical bone and reduced trabecular bone – increased bone turnover.

70
Q

psych s/s hyperthyroid

A

thyrotoxicosis will have agitation, psychosis, depression, anxiety, restlessness, irritable, insomnia

71
Q

geriatric hyperthyroid

A

apathetic not hyperactive with tremors but have a higher prevalence of weight loss, SOB and afib

72
Q

hyperthyroid with a normal or high RAI uptake indicates

A

de novo synthesis of hormone (normal creation of hormone from a molecular form) treat with a thionamide such as methimazole which will interfere with this synthesis

73
Q

hyperthyroid with near absent RAI indicates

A

inflammation and destruction of thyroid tissue with release of preformed hormone into circulation or an extrathyroidal source of thyroid hormone. Thyroid hormone is not being actively synthesized due to the inflammation and thionamide therapy (methimazole) is not helpful

74
Q

hyperthyroid is more common in men or women?

A

women 5:1, also more common in smokers.

75
Q

graves most common in

A

young women

76
Q

toxic nodular goiter more common in

A

older women

77
Q

disorders causing a normal or high RAI

A

de novo synthesis –> graves, hashitoxicosis, toxic adenoma, toxic multinodular goiter, iodine induced hyperthyroidism, trophoblastic disease and germ cell tumors,TSH mediated hyperthyroidism, epoprostenol

78
Q

Graves disease definition

A

Most common cause of hyperthyroidism. Autoimmune resulting from TSH antibodies/Thyroid stimulating immunoglobulins stimulating thyroid growth and thyroid hormone synthesis.

79
Q

Risk factor for Graves

A

high iodine intake, stressful life events

80
Q

Hashitoxicosis

A

hashimoto plus thyrotoxicosis autoimmune thyroid disease presenting with hyperthyroid and a high radioiodine uptake caused by TSH antibodies similar to Graves leads to hypothyroidism by the lymphocytes and autoimmune destruction of the thyroid tissue similar to Hashimotos Thyroiditis

81
Q

Toxic Adenoma and Toxic Multinodular Goiter

A

focal or diffuse hyperplasia of the of thyroid follicular cells who produce TSH from somatic mutations of genes. Mutation of the TSH receptor gene is the most common. Common in areas where iodine intake is relatively low.

82
Q

Iodine induced hyperthyroidism

A

Can occur after an iodine induced CT or iodine rich drugs like Amiodarone

83
Q

Trophoblsatic disease and germ cell tumors

A

Women with hydatidiform mole or choriocarcinoma (both are tumors in the uterus) and men with testicular germ cell tumors directing stimulating the TSH receptors. Therapy directed at the tumor.

84
Q

TSH Mediated hyperthyroidism

A

neoplastic or nonneoplastic. Neoplastic are pituitary adenomas. Causes goiter and at times visual field defects and galactorhea. Tx is Octreotide and surgery,

85
Q

Hyperthyroidism with near absent rai uptake

A

Either inflammation or destruction of thyroid tissue or ingestion. – Thyroiditis (inflammation), ingestion of thyroid hormone, or Ectopic production of thyroid hormone (excess in circulation)

86
Q

Thyroiditis

A

Inflammation of thyroid tissue with transient hyperthyroidism due to hormone release from the colloids space followed by hypothyroidism and recovery,

87
Q

Subacute granulomatous thyroiditis

A

viral or post viral syndrome characterized by fever, malaise, and a very painful goiter

88
Q

Silent thyroiditis or Subacute lymphocytic thyroiditis

A

autoimmune, painless, can occur postpartum usually

89
Q

Chemical thyroiditis

A

from amiodarone, meds ending in ‘nib’ –> destruction, lithium

90
Q

Therapy for thyroiditis

A

symptom control w betablockers, antiinflammatory drugs like aspirin, NSAIDs, and if severe - prednisone

91
Q

Exogenous and ectopic hyperthyroidism

A

Hyperthyroidism resulting from excess thyroid hormone originating from outside the thyroid gland from ingestion of hormone, levothyroxine overdose, ovarian neoplasm called struma ovarii, or thyroid cancer mets

92
Q

in osteitis fibrosa cystica, brown tumors of long bones result from what? What is the brown color from?

A

excess osteoclast activity; brown color is due to hemosiderin deposition.

Primary Care 3 (29 decks)

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